Ankylosing spondylitis (AS) is a chronic, progressive, inflammatory disease with considerable impact on patient functioning, well-being, and disability. The prevalence of AS has traditionally been estimated in the range of 0.1-1.9%, with more males affected than females (Sieper et al. Ann Rheum Dis 2001; 60:3-18; Silman & Hochberg Rheum Dis Clin North Am 1996; 22:737-49; Gran & Husby, Semin Arthritis Rheum 1993; 22(5):319-34). Millions of people are affected by ankylosing spondylitis (AS). As a chronic disease of the axial skeleton and large peripheral joints, AS causes inflammatory back pain and stiffness and it is associated with other inflammatory diseases of the skin, eyes and intestines. AS is difficult to diagnose in its early stages and is often an overlooked cause of persistent back pain in young adults.
As the disease progresses, patients with AS experience pain, joint stiffness, and the eventual loss of spinal mobility. These clinical symptoms and subsequent disease progression result in functional limitations, as well as impairment in health-related quality of life (Dagfinrud et al. Ann Rheum Dis 2004:63:1605-10; Bostan et al. Rheumatol Int 2003; 23:121-6; Zink et al., J Rheumatol 2000; 27:613-22; Ward 1998, Rheum Dis Clin North Am 1998; 24:815-27). In severe cases, AS may result in complete spinal fusion, causing extreme physical limitation.
No cure exists for AS. Traditionally, there were only a limited number of treatments available for ankylosing spondylitis (AS), including nonsteroidal anti-inflammatory drugs (NSAIDs) and physiotherapy. NSAIDs and physiotherapy provide symptomatic relief but do not affect disease activity or progression in AS. Traditional disease-modifying antirheumatic drugs (DMARDs), such as methotrexate and sulfasalazine, have demonstrated only limited effectiveness. Generally, treatment includes trying to relieve pain and stiffness using medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying antirheumatic drugs (DMARDs). In recent years, biologic response modifiers that inhibit TNF activity have become additional therapies for treating AS, as tumor necrosis factor (TNFα) is present in increased concentrations in joints.